Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway

Abstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., f...

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Main Authors: Feng Liang, Xin Fu, Yunpengfei Li, Fanglei Han
Format: Article
Language:English
Published: SpringerOpen 2020-09-01
Series:AMB Express
Subjects:
Online Access:http://link.springer.com/article/10.1186/s13568-020-01105-4
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author Feng Liang
Xin Fu
Yunpengfei Li
Fanglei Han
author_facet Feng Liang
Xin Fu
Yunpengfei Li
Fanglei Han
author_sort Feng Liang
collection DOAJ
description Abstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., for 21 days after ISF exposure. The protective effect of DOP was estimated by assessing cognitive function using the neurological score and the Morris water maze. Neuronal apoptosis was assessed in the hippocampus using the TUNEL assay, and protein expression of caspase-3, Bax, and Bcl-2 was measured by Western blotting. The levels of cytokines and oxidative stress parameters were assessed by ELISA. Western blotting and RT-PCR were performed to measure the expression of NF-kB, TLR-4, Sirt-1, and cyclin B1 protein in the brain. The cognitive function and neurological function scores were improved in the DOP group compared with the ISF group. Moreover, DOP treatment reduced the number of TUNEL-positive cells and the expression of caspase-3, Bax, and Bcl-2 protein in the brains of rats with neuronal injury. The levels of mediators of inflammation and oxidative stress were reduced in the brain tissue of the DOP group. Treatment with DOP attenuated the protein expression of TLR-4, NF-kB, cyclin B1, and Sirt-1 in the brain tissue of rats with neuronal injury. In conclusion, DOP ameliorates neuronal apoptosis and improves cognitive function in rats with ISF-induced neuronal injury. Moreover, DOP treatment can prevent neuronal injury by regulating the TLR-4/cyclin B1/Sirt-1 pathway.
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spelling doaj.art-a490088f566f495faccd58475acac4ac2022-12-22T01:14:52ZengSpringerOpenAMB Express2191-08552020-09-011011910.1186/s13568-020-01105-4Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathwayFeng Liang0Xin Fu1Yunpengfei Li2Fanglei Han3Department of anesthesiology, China-Japan Union Hospital of Jilin UniversityDepartment of anesthesiology, China-Japan Union Hospital of Jilin UniversityDepartment of anesthesiology, China-Japan Union Hospital of Jilin UniversityDepartment of anesthesiology, China-Japan Union Hospital of Jilin UniversityAbstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., for 21 days after ISF exposure. The protective effect of DOP was estimated by assessing cognitive function using the neurological score and the Morris water maze. Neuronal apoptosis was assessed in the hippocampus using the TUNEL assay, and protein expression of caspase-3, Bax, and Bcl-2 was measured by Western blotting. The levels of cytokines and oxidative stress parameters were assessed by ELISA. Western blotting and RT-PCR were performed to measure the expression of NF-kB, TLR-4, Sirt-1, and cyclin B1 protein in the brain. The cognitive function and neurological function scores were improved in the DOP group compared with the ISF group. Moreover, DOP treatment reduced the number of TUNEL-positive cells and the expression of caspase-3, Bax, and Bcl-2 protein in the brains of rats with neuronal injury. The levels of mediators of inflammation and oxidative stress were reduced in the brain tissue of the DOP group. Treatment with DOP attenuated the protein expression of TLR-4, NF-kB, cyclin B1, and Sirt-1 in the brain tissue of rats with neuronal injury. In conclusion, DOP ameliorates neuronal apoptosis and improves cognitive function in rats with ISF-induced neuronal injury. Moreover, DOP treatment can prevent neuronal injury by regulating the TLR-4/cyclin B1/Sirt-1 pathway.http://link.springer.com/article/10.1186/s13568-020-01105-4DesoxyrhapontigeninNeuronal injuryIsofluraneApoptosisTLR-4Sirtuin
spellingShingle Feng Liang
Xin Fu
Yunpengfei Li
Fanglei Han
Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway
AMB Express
Desoxyrhapontigenin
Neuronal injury
Isoflurane
Apoptosis
TLR-4
Sirtuin
title Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway
title_full Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway
title_fullStr Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway
title_full_unstemmed Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway
title_short Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway
title_sort desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane induced neuronal injury model by modulating the tlr 4 cyclin b1 sirt 1 pathway
topic Desoxyrhapontigenin
Neuronal injury
Isoflurane
Apoptosis
TLR-4
Sirtuin
url http://link.springer.com/article/10.1186/s13568-020-01105-4
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AT yunpengfeili desoxyrhapontigeninattenuatesneuronalapoptosisinanisofluraneinducedneuronalinjurymodelbymodulatingthetlr4cyclinb1sirt1pathway
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